Antithymocyte globulin
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First report of Hashimoto’s encephalopathy?: case report A 55-year-old woman developed Hashimoto’s encephalopathy after undergoing a kidney transplantation with antithymocyte globulin as induction immunosuppressive therapy. The woman, who had a 30-year history of type I diabetes mellitus and lymphomatous thyroiditis [Hashimoto’s thyroiditis], was found unresponsive at home. Two years previously, as a participant in a clinical trial (IRB# 286-03), she had undergone transplantation with a single dose of rabbit antithymocyte globulin 6 mg/kg administered over 24 hours; she had then received maintenance therapy with sirolimus and tacrolimus; after 6 months, tacrolimus was replaced by mycophenolate mofetil. On presentation, she had stiff and flexed extremities, with laboured breathing. Her blood glucose level was 60 mg/dL. Glucose was administered, but the woman’s condition did not change. An MRI showed mild to moderate hyperintensity in the brainstem and cerebral white matter. EEG showed frequent triphasic waves and rare sharp waves in the frontal central region, with a moderate to marked diffuse background. Analysis of a lumbar puncture identified an increased protein level in her cerebrospinal fluid (60 mg/dL). Levels of neuronspecific enolase, thyroid stimulating hormone and free triiodothyronine were 3.3 µg/L, 0.166 µIU/mL and 0.7 pg/mL, respectively. She had an increased level of antithyroid peroxidase antibodies (448 IU/mL); this, combined with the presence of encephalopathy with no other cause, met the criteria for diagnosis of Hashimoto’s encephalopathy. High dose prednisone was initiated on day 5 of hospitalisation; she became responsive within 24 hours and, within 1 week, regained motor skills and cognition. Within 2 weeks of prednisone initiation, her bowel and bladder function returned. She was discharged with full neurological and cognitive recovery, on day 24 of hospitalisation. A subsequent reduction in prednisone dosage resulted in a worsening tremor; this resolved completely on reinstatement of the prior prednisone dosage, at which she was subsequently maintained. Author comment: "[T]he possibility of [Hashimoto’s encephalopathy] risk increasing due to the use of lymphocyte-depleting induction regimens warrants further examination. . . Possibly the number of surviving regulatory T cells may be insufficient to inhibit the expansion of autoreactive T cell clones during homeostatic repopulation. . . [Additionally,] it may be that without [maintenance immunosuppression with] calcineurin inhibitors, expansion of self-reactive T cells might occur more easily". Stevens RB, et al. Hashimoto’s encephalopathy after intensive lymphocyte depletion with rabbit antithymocyte globulin in a renal transplant patient. American 801079515 Journal of Transplantation 8: 245-249, No. 1, Jan 2008 - USA
» Editorial comment: A search of AdisBase, Medline and Embase did not reveal any previous case reports of Hashimoto’s encephalopathy associated with antithymocyte globulin. The WHO Adverse Drug Reactions database contai
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